TENS mechanisms of action - sensory nerves
Sensory nerve stimulation: manage chronic or acute pain, aid relaxation and improve mobility
Sensory nerve stimulation
- Pain relief
- Release of muscle tension
Both analgesic pharmaceuticals and sensory nerve stimulation work by reducing pain related activity in the nervous system. Methods of pain relief that rely upon stimulation of sensory nerve fibres include:
- Thermal treatments
- Transcutaneous electrical nerve stimulation (TENS)
In clinical trials TENS has been shown to be as effective as acupuncture and more effective than massage, pressure and thermal treatments.
TENS compares very favourably with all the above in terms of convenience, reliability, ease of use, cost-effectiveness and because it can be used daily, for as long as needed - at home, or on the move.
How analgesic TENS works
TENS acts through two main mechanisms that help to alter and relieve the experience of pain:
- A peripheral mechanism known as Pain Gating
- Several central mechanisms that release many natural pain inhibiting chemicals
Pleasant sensations are carried by nerve fibres of large diameter and rapid signal conduction. Sharp pain is carried by medium width and medium speed nerve fibres. Dull or slow burning pain is carried by narrow, slow transmission nerve fibres.
The nociceptive system exists in one of 5 states:
- Pre-injury (healthy and ready to respond to actual tissue damage)
- Sensitized (injured and responding to protect the body from further damage)
- Persistently sensitized (dysfunctional and amplified)
- Re-organized (abnormal and amplified)
- Suppressed (abnormal and diminished)
A persistently sensitized or re-organized pain system results in chronic pain. There is no longer any underlying cause or tissue damage. Chronic pain is a disease in its own right.
The primary, peripheral pain relief mechanism has been termed “Gate Control Theory”. It was first proposed by Melzac and Wall in 1965 [“Pain mechanisms: a new theory”] and has been expanded and modified since. A simple explanation of the theory goes like this:
- Non-painful signals travel more quickly than painful signals
- They arrive at pain processing parts of the brain stem ahead of painful signals
- The non-painful signals activate sensory neurons (called WDR neurons)
- While the WDR neurons are "busy" processing pleasant signals, the painful signals cannot be received, processed or transmitted on to the central part of the brain
- The perception of pain is modulated - pain is relieved
Central mechanisms of action
Since 2010 brain imaging studies have been available. They show that TENS therapy affects pain-related cortical activation; specifically TENS:
- Inhibits pain activity in the spinal column, the brain stem and cortex
- Works when the pain system is sensitized (post injury), and when it is persistently sensitized or re-organized (chronic pain)
- Increases the pain threshold both during and after treatment; i.e. analgesic benefits last beyond the application time of the treatment
Beta-endorphin and encephalin are 2 of the human body's own naturally-occurring, pain-control hormones.
Evidence that natural opioids were involved in TENS analgesia first emerged in the 1970s. Later research determined that both beta-endorphin and met-encephalin levels are increased by TENS therapy.
- Beta-endorphin reduces pain, and promotes a feeling of well-being and relaxation
- Met-encephalin produces analgesia and anti-depressant-like effects
- Low-frequency TENS action is via beta-endorphin and μ-opioid receptors
- High frequency TENS action is via met-encephalin and spinal δ-opioid receptors
Other chemicals associated with TENS action
- GABA plays a role in the inhibition of pain. In 1995 it was demonstrated that GABA was elevated by high frequency TENS
- Serotonin is a neurotransmitter that reduces pain in the CNS. In 2006 it was demonstrated that 20 minutes of low frequency TENS increased central serotonin concentrations during and immediately after treatment
- Various studies have shown that stimulation using either high or low frequency TENS is associated with nor-adrenaline and thus pain inhibition
- Activation of spinal cholinergic receptors is anti-nociceptive. Certain receptor sub-types of acetycholine are released by TENS therapy, thus acting to prevent hyper sensitivity
- Aspartate and glutamate are associated with increased painful sensations and play a role in the sensitization of the pain system. High frequency TENS has been shown to reduce the release of aspartate and glutamate in the dorsal horn, thus helping to prevent a transition from acute pain to chronic pain
Summary of TENS analgesic benefits
- High frequency - Pain gating, increase of encephalin and GABA, decrease of aspartate and glutamate
- Low frequency - increase of beta-endorphin, serotonin, acetylcholine and nor-adrenaline
- Mixed frequency - by alternating the two frequencies and applying the therapy for as long as needed, mixed frequency TENS therapy can provide the benefits of all the above mechanisms of pain relief action
Basic TENS therapy was born in the 1970s. But in the 1990s there was a further breakthrough in the understanding of frequency specific benefits, mixed frequency benefits and accumulation of the TENS dose over time. Mixed frequency TENS and/or modulated single frequency TENS serve to avoid the problem of tolerance, once associated with early TENS results
Jim Lamers, together with the team at Bio Electronics and ActivLife Technologies, was at the forefront of TENS therapy development - always designing and manufacturing units based on the absolute latest research, with comfort and effectiveness of primary concern.